Nutrition in critical care

1. Nutrition in critical care Pratthana Srisangthong,MD

2. Scope • Metabolic response in critical illness • Assessment of nutritional status • Enteral nutrition • Parenteral nutrition • Immunonutrition and antioxidant

3. Background • Adequate nutrition is essential to the critically ill patient. • It helps support • anabolism • uncontrolled catabolism • maintain a competent immune system • improve patient outcome. • Severe trauma, burns, sepsis, and head injury are associated with marked hypermetabolism and hypercatabolism,  metabolic alterations.

4. Metabolic response in critical illness • 2 principal metabolic response • 1 response to starvation • 2 response to stress Proceedings of the Nutrition Society (2007), 66, 16–24

5. Metabolic response to starvation • Typical setting  patient with chronic disease • During the first 12 – 24 hr of acute starvation mobilization of hepatic glycogen stores • 24 – 72 hr stimulation of gluconeogenesis • After 72 hr - increase in hepatic ketone bodies production - reduction of gluconeogenesis - decreased protein breakdown • Subsequently, as starvation progresses decrease lean body mass and BMR Nutrition 13(Supp1):45S-51S, 1997

6. Metabolic response to starvation • Several features distinguish the metabolic response of starved, critically ill patients. • As starvation progresses • increased loss of lean body mass • energy expenditure is not decrease. • Continuation of starvation beyond 3 d • not accompanied by a stimulation of both ketogenesis and ketone body oxidation (with their normally concomitant suppression of gluconeogenesis and protein breakdown)

7. Metabolic response to starvation • Starvation in critically ill patients leads to accelerated protein-calorie malnutrition. • These alterations caused by inflammatory mediators.

8. Metabolic response to stress • 1 energy metabolism - increased REE

9. Metabolic response to stress • Factor influenced energy expenditure 1 effect of illness - stage and length of illness - fever < each 1 c increase 10 – 15% of EE> - pain , physical activity , agitation , abnormal posturing , increase muscle tone , seizure

10. Metabolic response to stress • 2. effect of treatment - cathecholamine  EE - beta blocker  EE - sedative drug  EE Supportive treatment can limit level of metabolism

12. Metabolic response to stress • 2 protein metabolism - protein catabolism > protein synthesis net negative nitrogen balance - loss of muscle mass and protein degradation in vital organ - immobilization causes atrophy of skeletal muscle negative nitrogen balance Nutrition Vol. 13, No. 9(Suppl), 1997

13. Metabolic response to stress • protein metabolism - movement of amino acid ( alanine, glutamine ) for gluconeogenesis decreased intramuscular of glutamine - BCAA metabolism - liver reprioritized protein synthesis positive acute phase protein ( CRP , alpha 1 antitrypsin ) negative acute phase protein ( albumin , prealbumin )

15. A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.

16. Consequences of protein catabolism

17. Metabolic response to stress • 3 carbohydrate metabolism - increased couterreguratory hormone and cytokines GH, cortisol, glucagon, cathecholamine IL-1, IL-6, TNF, LTS, prostanoids endogeneous glucose production - insulin resistance hyperglycemia

18. Metabolic response to stress • carbohydrate metabolism substrate of gluconeogenesis glycerol [ from adipose tissue ] alanine [ from skeletal muscle ] lactate [ from peripheral tissue and skeletal muscle ]

19. Metabolic response to stress • 4 lipid metabolism effect of catecholamines and cytokines mobilization of glycerol and free fatty acid increased lypolysis increased fatty acid oxidation reduced energy store

20. Metabolic response to stress • 5 Changes in endocrine system The response is essential for maintainance of cellular and organ hemeostsis - activation of hypothalamic pituitary adrenal axis - release cortisol from adrenal tissue

21. Metabolic response to stress • 6 fluid and electrolyte depending on the patient’s underlying medical problems, nutritional status, and drug or resuscitative therapy.

22. Assessment of nutritional status • History [ include medical, surgical and dietary history ] A history of acute or chronic weight loss or gain before hospital admission is an essential indicator of the patient’s nutritional status.

23. Assessment of nutritional status • 2 Anthropometric parameters unreliable and seldom used because the patient’s positioning and fluid status affect their accuracy. • 3. Visceral protein levels • affected by stress, fluid shifts, and other factors • limit their specificity and sensitivity.

24. Assessment of nutritional status • 4 Delayed hypersensitivity skin testing - limits in the critically ill patients - many nonnutritional factors such as acute hemorrhage, hypovolemic shock, surgery, and the use of steroids and immunosuppressants depress immune function. • 5 Gold standard indirect calorimeter

25. Purpose of nutrition support • 1 safe life • 2 speed recovery by reducing neuropathy and maintain muscle mass and function

26. Route of supplement • EN vs PN Patients who can be fed via the enteral route should receive EN • Indication of EN in ICU patients All patients who are not expected to be on a full oral diet within 3 days should receive EN Clinical Nutrition (2006) 25, 210–223

27. Is early EN (< 24–48 h after admission to ICU) superior to delayed EN in the critically ill?

28. Effects of Early Enteral Feeding on the Outcome of Critically Ill Mechanically Ventilated Medical Patients* large multi-institutional ICU database. 4,049 patients requiring mechanical ventilation for > 2 days. overall ICU and hospital mortality were lower in the early feeding group (18.1% vs 21.4%, p 0.01 early feeding was found to be independently associated with an increased risk of ventilator-associated pneumonia (VAP)

29. Effects of Early Enteral Feeding on theOutcome of Critically Ill MechanicallyVentilated Medical Patients* CHEST / 129 / 4 / APRIL, 2006

30. Prospective ,controlled, clinical trials - 150 patients were enrolled. 75 pt  early feeding 75 pt  late feeding • Patients in early feeding had greater incidence of VAP.[49.3% vs 30.7% p 0.020] and longer ICU days. • No statistic difference in mortality • Aggressive early EN in mechanical ventilator medical patients is associated with greater infection and prolong length of stays.

32. Is early EN (<24–48 h after admission to ICU) superior to delayed EN in the critically ill? The expert committee, however favours view that critically ill patients, who are haemodynamically stable and have a functioning gastrointestinal tract, should be fed early (< 24 h), if possible, using an appropriate amount of feed

33. How much EN should critically ill patients receive? - During the acute and initial phase of critical illness an exogenous energy supply in excess of 20–25 kcal/kg BW/day may be associated with a less favourable outcome - During recovery (anabolic flow phase), the aim should be to provide 25–30 total kcal/kg BW/day

34. How much EN should critically ill patients receive? Patients with a severe undernutrition should receive EN up 25–30 total kcal/kg BW/day. If these target values are not reached supplementary parenteral nutrition should be given.

35. Caloric Intake in Medical ICU Patients* • Prospective cohort study. • Patients with an ICU length of stay of at least 96 hr. • Study participants were underfed relative to ACCP targets. moderate caloric intake (9 to 18 kcal/kg per day) was associated with better outcomes than higher levels of caloric intake. CHEST / 124 / 1 / JULY, 2003

36. Which route is preferable for EN? • There is no significant difference in the efficacy of jejunal versus gastric feeding in critically ill patients

37. Protein requirement • 1.5 g/kg/day. • 2 g/kg/day in patients with trauma, severe burns, and head injury • 2.5 g/kg/day in adult patients treated with continuous renal replacement therapy (CRRT) • nutritional support can only limit the loss of the body’s protein and calorie stores. • The goal is to administer sufficient nitrogen to provide a positive or neutral nitrogen balance.

38. Lipid requirements • 0.5 – 1 g/kg/d [ 20-40% of energy ] • Lipid clearance is reduced in stressed patients due to decreased activity of lipoprotein lipase (LPL), • infusion rate should not exceed 0.12 g/kg/hr to avoid the development of elevated triglyceride levels. • Source of essential fatty acid, fat soluble vitamin. • Avoid omega 6 [ linoleic is precursor of arachinodic acid precursor of PG,TXA,LT ]

39. Lipid requirements • 0.5 – 1 g/kg/d [ 20-40% of energy ] • Lipid clearance is reduced in stressed patients due to decreased activity of lipoprotein lipase (LPL), • infusion rate should not exceed 0.12 g/kg/hr to avoid the development of elevated triglyceride levels. • Source of essential fatty acid, fat soluble vitamin. • Avoid omega 6 [ linoleic is precursor of arachinodic acid  precursor of PG,TXA,LT ]

40. Parenteral nutrition Indication • In patients who cannot be fed sufficient enterally the deficit. • intolerant to EN Beware • Overfeeding • PN should not be used to correct acute fluid and electrolyte deficienciesใ

41. Complications of PN • PN associated with a more pronounced proinflammatory response than EN harmful in patients with severe inflammation. • Complications of excess dextrose infusion hyperglycemia hypertriglyceridemia hepatic steatosis, respiratory decompensation depression of immune function

42. Complications of PN Hyperglycemia • depression of immune function • increase infection risk • impair cellular and humoral host defenses • reducing phagocytosis • inhibiting • complement fixation Controlling hyperglycemia has resulted in improved phagocytic function as well as improved patient outcome.

44. n engl j med 355;18 november 2, 2006

45. Complications of PN Hypertriglyceridemia • due to dextrose overfeeding or excess lipid infusion. • Stressed patients are at higher risk for hypertriglyceridemia due to 1 increased lipolysis and hepatic fatty acid reesterification 2 increased hepatic triglyceride synthesis from dextrose infusion 3 decreased LPL enzyme activity 4 medications such as corticosteroids

46. Complications of PN • Hypertriglyceridemia • Patients at risk sepsis multiorgan failure diabetes liver disease renal failure pancreatitis.

47. Complications of PN • hypercapnia -result from total energy and dextrose overfeeding • patient at risk borderline respiratory function and limited pulmonary reserve. • excess carbon dioxide is produced • increased respiratory workload and minute ventilation

48. Immunonutrition and antioxidant • Growth hormone • Arginine • Antioxidant • Selenium

49. The negative nitrogen balance in critically ill patients is partly due to resistance to growth hormone and the decreased production and action of IGF-I • prospective, multicenter, double-blind, randomized, placebo-controlled trials • 247 Finnish patients and 285 patients in other European countries who had been in an ICU for 5 to 7 days N engl j med 355;18 www.nejm.org november 2, 2006

50. The in-hospital mortality rate was higher in the patients who received growth hormone than in those who did not (P<0.001) • Among the survivors, the length of stay in ICU and in the hospital and the duration of mechanical ventilation were prolonged in the growth hormone group. • In patients with prolonged critical illness, high doses of growth hormone are associated with increased morbidity and mortality.